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Updated: Oct 8, 2026
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Identification and validation of genes associated with mitochondria in cerebral infarction and benign prostatic
Hongjian Tu1, Shanzhi Zhan1, Leihua Cao1
1Department of Urology, Nanchang People's Hospital, Nanchang, China.
Background:
Cerebral infarction (CI) and benign prostatic hyperplasia (BPH) are prevalent conditions in middle-aged and elderly individuals. Previous studies have demonstrated that mitochondrial dysfunction plays a critical role in both CI and BPH. This study aims to identify the mitochondria-related genes (MRGs) in CI and BPH, providing theoretical clues and preliminary candidate gene resources for further research on mitochondria targeted therapeutic strategies across different diseases.
Methods:
The transcriptomic data of BPH and CI were obtained from public databases, while MRGs were derived from published literature. Firstly, the differentially expressed genes (DEGs) in the combined and batch-effect-removed datasets were intersected with MRGs to obtain candidate genes, and their functions were explored. Then, hub genes were further screened through machine learning. Subsequently, the expression levels of hub genes, their predictive abilities for diseases, and the changes in the immune microenvironment were respectively analyzed in the relevant datasets of BPH and CI. Finally, RT-qPCR was used to verify the expression of hub genes in humans.
Results:
Eleven candidate mitochondrial genes were identified. They likely mediated CI and BPH pathogenesis via metabolic and cellular regulation. Further analysis showed that HSDL2 and PDK4 were downregulated in BPH, enabling effective BPH-control discrimination. The nomogram constructed based on these two genes also had a strong predictive ability for the risk of developing BPH. CYP1B1, GYG1, HSDL2, MXD1, SLC22A4, and TNFSF10 were significantly upregulated at high levels in the disease group and had a strong ability to distinguish between CI and control samples. The nomogram constructed based on these six genes showed a strong predictive ability for the risk of developing CI. In addition, activated B cells and neutrophils showed opposite infiltration trends in BPH and CI relative to healthy controls. Finally, RT-qPCR confirmed that the expression of HSDL2 and PDK4 in patients with comorbid CI and BPH (CIwPH) was significantly lower than that in normal controls.
Conclusion:
This study identified 8 hub genes and explored their application value in clinical identification, providing new research directions for the diagnosis and treatment of BPH and CI.
